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Absence of oncogenic transformation despite acquisition of cytogenetic aberrations in long-term cultured telomerase-immortalized human fetal hepatocytes.

作者信息

Haker Björn, Fuchs Sigrid, Dierlamm Judith, Brümmendorf Tim H, Wege Henning

机构信息

Department of Gastroenterology and Hepatology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany.

出版信息

Cancer Lett. 2007 Oct 18;256(1):120-7. doi: 10.1016/j.canlet.2007.06.007. Epub 2007 Jul 13.

DOI:10.1016/j.canlet.2007.06.007
PMID:17630152
Abstract

As a culture model to study hepatocarcinogenesis, telomerase-immortalized human fetal hepatocytes were monitored for karyotype changes evolving in long-term culture and development of functional defects in DNA damage response. G-banding revealed acquisition of characteristic karyotype abnormalities, e.g., trisomy 7 and monosomy X, in two independently immortalized and cultured populations after 80-100 population doublings. Interestingly, the detected aneuploidies resemble some of the genetic events observed in hepatocellular cancer. However, these genetic changes were not sufficient to induce oncogenic transformation reflected by absence of anchorage-independent growth. Furthermore, long-term cultured telomerase-immortalized cells preserved p53 expression levels and effective p53-mediated damage response.

摘要

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